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275 Cards in this Set
- Front
- Back
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What are the developmental disorders of kidney?
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- Bilateral agenesis
- Unilateral agenesis - Malformations - Cystic dysplasia |
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Consequences of bilateral agenesis?
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No urine prod - oligohydramnion - Potter face and often death by lung underdevelopment
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What happens to second kidney in unilateral agenesis?
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Compensatory hyperplasia
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Typical malformations of kidneys?
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Fusion of poles:
- Horse-shoe - S-shaped |
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What is cystic dysplasia of kidney?
Another name for it is? |
Developmental disorder of fetus - with unsuccessful fusing of the nephric ducts
So the urine is still filtrated in glomeruli - but it has nowhere to go - so tubules with cystically dilate. Another name = Multicystic renal dysplasia NB! This is NOT polycystic kidney disease :)) |
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How is histology of a cystic dysplasia of kidney?
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- Cysts and ducts
- Smooth muscles - Fibrous tissue - Also bone & cartilage (!!) Since there is islands of immature mesenchyme found between the cysts - which develop:) |
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Treatment of cystic kidney dysplasia?
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Removal of affected kidney & dialysis if necessary
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How does cystic renal dysplasia affect kidneys?
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Here and there in one or both kidneys
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What renal cystic disorders do we have?
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- Simple renal cysts (most common)
- ARPDK - ADPDK |
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What is a simple renal cyst?
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- Single or multiple, small (mm) or larger (cm) cyst
- Filled by clear fluid, which flattens epithelium Not dangerous, usually found in searching for something else |
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ARPKD means?
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Autosomal recessive polycystic kidney disease - very rare!
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Gross morphology of kidney in ARPKD?
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Enlarged
Multiple tiny cysts |
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Infant anatomy in ARPKD?
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1. Oligohydramnion
- Potters face 2. Huge stomach - Pulmonary hypoplasia (death) - since kidney is pushing organs (diaphragm) |
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Usual prognosis of ARPKD?
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1. Stillborn (pulmonary / renal failure)
2. If survive: - Concentration disorder + uremia |
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What is ADPKD?
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Adult polycystic kidney disease
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How does ADPKD develop?
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We don't know - it just manifest in 3rd of 4th decade of life
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How does ADPKD develop symptomatically?
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1. Cyst grow slowly, it destroys glomeruli so the filtrate is captured.
2. Cause pain, tension and hematuria if cysts rupture. |
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How many % of nephrons are affected in ARPKD?
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100%
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How many % of nephrons are affected in ADPKD?
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50%
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Gross morphology of ADPKD?
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Very large - 30 cm and 1-3 kg!
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Size of ADPKD cysts?
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Many cm large
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How does ADPKD look in LM?
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Larger cysts from any part of nephron
No parenchyma preserved more or less |
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ADPKD is often accompanied by what diseaes?
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1. Bile duct cysts
2. Pancreatic duct cysts 3. Cerebral artery aneurysm! |
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Definition diffuse glomerular injury?
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Damage of >80% of glomeruli
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Definition focal glomerular injury?
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Damage of some <80% of glomeruli
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Definition global glomerular injury?
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Damage of all glomeruli
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Definition segmental glomerular injury?
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Damage to part of the glomeruli
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By what 4 things does a glomeruli react to injury?
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1. Proliferation of cells
2. Exsudation 3. Thickening of BM 4. Sclerotization ==> So you see it tries to adapt to some stimuli! |
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What cells proliferate in glomerular injury?
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1. Mesangial cells (+matrix)
2. Endothelial cells 3. Bowman capsule cells |
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The exudate in glomeruli injury consist of?
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- Leukocytes
- Monocytes - Protein - Fibrin - Crescents |
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What is usually the cause of thickened BM in glomerular injury?
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Immune complex deposition
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What does sclerotization of glomeruli mean?
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Deposition of mesangial matrix - so glomeruli becomes harder
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Glomerular diseases - which side do they usually affect?
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ALWAYS bilateral :)
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2 groups of glomerular injuries?
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1. Immune injury
2. Non-immune injury |
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What are the immune injuries to glomeruli?
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1. Circulating complexes
2. In situ immunocomplexes 3. Autoantibodies to BM 4. ANCA |
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From what does the Ab-Ag complexes that damage the glomeruli?
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From:
- Viruses - Strep - SLE |
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How does the immune complexes damage glomeruli?
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By getting trapped in:
- Mesangium - BM |
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What is the mesangium?
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A thin membrane of mesangial cells, which are supporting the capillary loops of the renal glomeruli
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How to detect immune complexes in glomeruli?
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Immunofluorescence
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What are the in situ immune complexes - and what are they called?
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First - antigens attach to glomerular structures
Later - antibodies bind them and create complexes This is called 'deposits' |
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Example of disease with autoantibodies against glomerular BM?
What structure in BM is the antibodies against? |
Goodpasture syndrome - autoantibodies against Collagen IV
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How does immune complexes look in immunoflyorescence?
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Granular positivity
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How does autoantibody disease look in immunofluorescence?
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Linear positivity
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What does ANCA mean?
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Anti neutrophilic cytoplasmic antibodies
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What is the main lesions caused by ANCA?
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Vasculitis
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How does ANCA cause vasculitis?
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1. Houndreds of ANCA's attack neutrophils
2. Which causes neutrophils to attack vessel walls with complement activation & enzymes (imagine a whole bunch of birds taking down a plane - and it crash-lands and destroy the ground) |
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What are the non-immunological injuries to kidney glomeruli?
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1. Loss of negative BM charge
2. Hyperfiltration 3. Hereditary defect of BM 4. Glomerular ischemia |
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What causes the loss of negative charge on BM - and what is the consequence?
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T-cell cytokines - proteins escape
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What is the consequence of hyperfiltration in glomeruli+
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1. Glomeruli number reduced
2. Proliferation of mesangial cells and matrix 3. Sclerosis - which again decrease number of glomeruli |
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Name 2 hereditary syndromes with defect of glomeruli BM?
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1. Alport syndrome
2. Thin BM syndrome |
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Result of glomeruli ischemia?
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Collapse and sclerosis
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What is a primary glomerulonephritis?
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The immune based damages of glomeruli
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What is a secondary glomerulonephritis?
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The damage of glomeruli in systemic disorders:
- SLE - Vasculitis - DM - Amyloidosis - Endocarditis |
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Definition nephrotic syndrome?
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A kidney disease mostly characterized by loss of protein into urine due to increased permeability - and subsequent edema
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What is proteinuria for nephrotic syndrome?
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<3.5g / 24h
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What are the biochemical signs of nephrotic syndrome?
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1. Hypoalbuminemia
2. Hyperlipidemia |
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Why is there hyperlipidemia in nephrotic syndrome?
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Compensatory overproduction of cholesterol - along with increaed albumin production
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What are the 4 primary diseases commonly causing nephrotic syndrome?
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1. Minimal change disease
2. Membranous glomerulopathy 3. Focal segmental glomerulosclerosis 4. Membranoproliferative glomerulonephritis |
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What are the common systemic (secondary) diseases causing nephrotic syndrome?
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- SLE
- DM - Amyloidosis |
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What is minimal change disease?
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Glomerular disorder with loss of epithelial foot processes of podocytes (seen in EM) - leading to selective proteinuria and edema
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What is etiology of minimal change disease?
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No one knows
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What do we see in LM of minimal change disease?
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Nothing - hence the name
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What is the selective proteinuria in minimal change disease?
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Only small proteins can escape - albumins.
Globulins stays!! |
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Typical age for minimal change disease?
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Young preschool children
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Definition membranous glomerulopathy?
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Presence of immune complexes / deposits in BM - leading to proteinuria
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What is the cause of membranous glomerulopathy?
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1. Mostly idiopathic
2. SLE, drugs, hepatitis B |
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How is histology of membranous glomerulopathy?
What is the special staining method? |
Thickened BM
Special staining = Jones method |
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What is Jones method?
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Normal BM is stained, but deposits not, so we see 'holes'
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Immunofluorescence of membranous glomerulopathy?
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Granular positivity
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Definition FSGS?
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A syndrome of focal sclerosis of parts of glomeruli - leading to nephrotic syndrome
"Focal sclerosing glomerulosclerosis" |
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Causes of FSGS?
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Unkown
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Symptom of FSGS?
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Non-selective proteinuria - Both:
- Globulins - Albumins |
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Histology of FSGS?
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Focal sclerosis of some glomeruli (= some amorphous matrix looking stuff)
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EM of FSGS?
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Loss of podocyte processes...
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Prognosis of minimal change disease?
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Very good
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Prognosis of membranous glomerulopathy?
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50%
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Prognosis of FSGS?
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Quite bad - renal failure in 10 years
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Definition membranoproliferative glomerulonephritis?
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Glomerulonephritis with:
1. Thickening of BM 2. Proliferation of mesangial cells 3. Increased mesangial matrix Due to some subendothelial deposits |
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Prognosis of MPGN?
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Quite poor - 100% recurrence after transplantation :/
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Definition nephritic syndrome?
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A syndrome comprising:
- Nephritis - Hematuria - Hypertension - Renal failure (and sometimes proteinuria) |
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Blood biochemistry signs of nephritic syndrome?
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Azotemia
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Urine biochemistry signs of nephritic syndrome?
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- Hematuria
- Oliguria - Mild proteinuria |
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What may the proteinuria be in nephritic syndrome?
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0.5-1g / 24h
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What are the common causes of nephritic syndrome?
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1. Acute proliferative glomerulonephritis
2. Rapid progressive nephritic syndrome 3. IgA nephropathy 4. Henoch-Schönlein purpura glomerulonephritis |
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What is acute proliferative glomerulonephritis?
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Nephritic syndrome occuring 1-3 weeks after b-hemolytic streptococcal infection (without ATB treatment)
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What is pathogenesis of acute proliferative glomerulonephritis?
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Huge immune complex deposition under BM
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Immunofluorescence of acute proliferative glomerulonephritis?
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Granular positivity
C3 + IgG positivity |
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Histology of acute proliferative glomerulonephritis?
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1. Enlarged, hypercellular glomeruli
--> Like it is pushed through the bownmans membrane |
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Prognosis of acute proliferative glomerulonephritis?
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Quite good :)
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What is RPGN?
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Rapidly progressive glomerulonephritis
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Another name for RPGN?
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Crescentic glomerulonephritis
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RPGN is manifested by?
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1. Hematuria
2. Proteinuria 3. Rapid loss of renal functions (weeks) if untreated |
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What is a crescent and what does it consist of?
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It is a halfmoon seen in glomeruli, consisting of:
- Fibrin - Monocytes - Bowman capsule cells |
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How does the crescents develop?
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1. Severe injury to capillary BM by enzymes of leukocytes & macrophages
2. Leakage of fibrin & blood cells into Bowman's space |
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How many of gomeruli are crescentic in rapidly progressive glomerulonephritis?
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50% ish
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What are the 3 stages of a crescent life?
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1. Cellular crescent - Only cells and good treatment
2. Fibrocellular crescents - and some fibroblasts 3. Fibrous crescents - only fibrous tissue and fibrocytes - no treatment response = end stage |
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What are the 3 main causes of rapidly progressive glomerulonephritis?
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1. Autoantibodies against BM (goodpasture)
2. ANCA vasculitis |
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What are the types of ANCA vasculitis attacking the kidney glomeruli?
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1. Wegener (granulomatosis with polyangitis)
2. Micro-polyangitis 3. Churg-Strauss syndrome |
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Which vasculitis avoid kidneys?
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Polyarteritis nodosa
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What is prognosis of rapidly progressive glomerulonephritis?
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Depends on stage of crescents :)))
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What is IgA nephropathy?
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A glomerulonephritis with deposits of IgA in mesangium of glomeruli (not BM!) - occuring after respiratory infections
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Clinical presentation of IgA nephropathy?
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1. Gross hematuria
2. Mild proteinuria |
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Histology of IgA nephropathy?
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1. Proliferation of mesangial cells
2. Glomerulosclerosis after many years (renal failure) |
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Immunofluorescence of IgA nephropathy?
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Granular positivity
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What is Henoch-Schönlein purpura?
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A systemic inflammation of blood vessels
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HS purpura manifest as?
Skin Joints GIT Kidneys |
Skin
- Purpuric rash Joints - Arthritis GIT - No idea Kidney - Nephritis syndrome (GN) |
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GN in HS-purpura looks how in histology?
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Very similar to IgA nephropathy - probably they are the same in the opposite sides of the spectrum.
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What is SLE - and what to do with kidney?
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A autoimmune disease with autoantibodies against DNA - affect kidney in almost all cases
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Clinical manifestations of lupus nephritis?
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- Hematuria
- Proteinuria - Nephrotic / nephritic syndrome Depends on type! |
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What are the 5 types of lupus nephritis according to WHO?
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1. Minimal mesangial glomerulonephritis
2. Mesangial proliferative glomerulonephritis 3. Focal proliferative glomerulonephritis 4. Diffuse proliferative glomerulonephritis 5. Membranous nephritis |
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How does infectious endocarditis affect kidneys?
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Immune complexes lead to focal glomerulonephritis with necrosis of parts of glomeruli
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Kidney involvement in AA vs. AL amyloidosis?
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AA = 100%
AL = 90% |
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Histology of kidney amyloidosis?
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Amorphous material in glomeruli and vessel interstitium
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How to stain for amyloid?
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Congo red
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EM of amyloid?
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Fibrils - especially in mesangium
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Clinical manifestatino of amyloidosis of kidney?
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Proteinuria . This may be first manifestation of amyloidosis!
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What are 2 hereditary nephropathies - affecting glomerular BM?
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1. Alport syndrome
2. Thin BM glomerulopathy |
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What is Alport syndrome?
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X-linked renal disease starting in childhood and leading to renal failure at 40 years due to glomerulosclerosis
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Clinical symptoms of Alport syndrome?
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1. Hematuria
2. Porteinuria after 20 years |
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Histology of alport syndrome?
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1. Mesangial proliferation
2. Later glomerulosclerosis |
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Which gender is worsely affected by alport syndrome?
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Males - females do not get renal failure
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What is happening at the BM of Alport syndrome?
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Areas of thick and thin BM - and some areas where lamina densa is splitted!
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What is thin BM glomerulopathy?
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Disease where BM thickness if half of what is should be (should be 350nm)
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Prognosis of thin BM glomerulopathy?
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Very good, only hematuria is problem
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What is maybe the most common renal syndrome?
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Recurrent and persistent hematuria - with no other nephritic symptoms
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What is the advanced stage of most glomerular disorders?
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Sclerosis and hyalinization of glomeruli - leading to slowly developing uremia and renal failure
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What is treatment of renal failure?
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Hemodialysis until transplantation can be done
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What is the name of the syndrome of end stage kidney?
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Chronic sclerosing glomerulonephritis
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At end stage kidney disease - are we able to detect primary disease?
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No
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Gross appearance of chronic sclerosing glomerulonephritis?
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- Small kidneys
- Weighing only 100g in total! - Granulated (many small corns on surface) |
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What are the main histological signs of chronic sclerosing glomerulonephritis?
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1. Up to global glomerulosclerosis
2. Interstitial fibrosis 3. Tubule atrophy (thyroidization) 4. Arteriole sclerosis and narrowing 5. Chronic lymphocytic infiltrate |
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Why do we call tubule atrophy for thyroidization of kidney?
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Since inside we find colloid-like material which is some proteinaceous fluid
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Why is there sclerosis and narrowing of the arterioles in end stage kidney?
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1. Hypertension due to:
2. Retention of water and ions |
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Definition pyelonephritis?
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Bacterial suppuratiev inflammation of kidney and pelvis
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Most frequent bacteria causing pyelonephritis?
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E.coli
Proteus Enterobacter Klebsiella |
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2 routes of infection causing pyelonephritis?
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1. Ascending
2. Hematogenous |
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How does bacteria enter in ascending route?
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1. Lower UTI (rectum --> Urethra)
2. Female |
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Lower UTI reaching urinary bladder is called?
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Urocystitis
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Urocystitis is very typical for?
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- Stones
- Gravidity - Bladder dysfunction (urine is left) - Diabetes |
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How can urine flow from bladder to ureter?
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Vesicourethral reflux (VUR)
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What is the main causes of VUR?
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1. 90 deg entering angle of urethra (congenital)
2. Inflammations 3. Stones |
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Inflammation of pelvis is called?
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Pyelitis
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How does the inflammation reach the kidney parenchyma?
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Through open collecting ducts in papillae
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What is the most important histological sign in ascending pyelonephritis?
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Longitudinal abscesses from medulla to cortex!
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Other histological signs of ascending pyelonephritis?
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In tubules
- Bacteria and leukocyte infiltrate - Destruction of tubules by purulent inflammation |
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How does bacteria enter kidney parenchyma from hematogenous route?
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From left heart in infective endocarditis
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Gross appearance of hematogenous pyelonephritis?
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1. Bilateral always
2. Many dot-like abscesses |
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Histology of hematogenous pyelonephritis?
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You see bacterial colonies in glomeruli
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What are the main complications of pyelonephritis?
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1. Necrotizing papillitis (DM)
2. Pyonephros 3. Perinephritic abscesses 4. Paranephritic abscesses 5. Urosepticemia |
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What is necrotizing papillitis?
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Necorsis of tips of papillae - since they are most sensitive
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What is pyonephros?
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Pelvis space filled by pus
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What is perinephritic abcsess?
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Presence of pus between kidney and capsule (abscess from cortex easily spread here)
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What is paranephritic abscess?
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Abscess in perinephritic fat
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What are the clinical manifestations of pyelonephritis?
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- Sudden costovertebral angle pain
- Fever & chills - Dysuria - Bacteruria (bacteria in lab) - Pyuria (leukocytes in lab) |
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What are the 2 main causes of chronic pyelonephritis?
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1. Chronic obstruction
2. Chronic reflux Both leading to repeated acute inflammations |
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What are the typical chronic obstructions of urinary tract?
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- Stones
- Prostatic hyperplasia |
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What is the main gross finding in chronic pyelonephritis?
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- U shaped scars on surface of kidneys
- Blunted calyces - due to healing of inflammation with scarring |
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Main histological findings in chronic pyelonephritis?
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1. Extreme lymphocytic infiltrate
2. Interstitial fibrosis 3. Dilation & thyroidization of tubules (atrophy) 4. Late glomerulosclerosis |
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What is chronic reflux associated pyelonephritis?
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Pyelonephritis caused by VUR - typical for children
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Gross kidney appearance chronic reflux pyelonephritis?
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Scarring on poles
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What are the interstitial nephropathies you know?
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- Acute drug-induced tubulointerstitial nephropathy (TIN)
- Analgesic nephropathy - Hepatorenal syndrome - Myeloma cast nephropathy - Radiation nephropathy |
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What is acute drug induced tubulointerstitial nephropathy?
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Allergic response to a drug:
- ATB, diuretics, NSAIDs + many others |
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What is manifestatino of acute drug induced tubulointerstitial nephropathy?
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1. Sudden fever with skin rash
2. Eosinophilia in blood (allergic) |
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Histology of acute drug induced tubulointerstitial nephropathy?
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1. Interstitial edema
2. Non-purulent inflammation of: - Lymphocytes - Eosinophils |
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What is analgesic nephropathy?
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Chronic TIN (tubulointerstitial nephropathy) and papillary necrosis due to long term hyperusage of analgesics
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Which analgesic is the worst for analgesic nephropathy?
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Phenacetin
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Histiological appearance of analgesic nephropathy?
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1. Interstitial scarring
2. Necrotic papillae WITHOUT leukocyte reaction 3. Tubular atrophy 4. Inflammation of parenchyma |
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Gross appearance analgesic nephropathy?
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1. Small atrophic kidneys
2. Black necrotic papillae - which may break off and block ureter --> hydronephrosis |
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What is the first step in hepatorenal syndrome?
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There must be some damage to liver parenchyma (necrosis, cirrhosis, toxic damage etc.)
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But what is so special about hepatorenal syndrome?
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1. Nobody knows how it happens
2. Mechanism of renal failure is unknown 3. But kidney can still be transplanted and work perfectly fine |
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What do we see in tubules in hepatorenal syndrome?
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Bile - but kidney tissue look almost normal!
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How may a multiple myeloma cause renal failure?
|
Via myeloma cast nephropathy:
- Produce light chains which form Bence-Jones proteins in the tubules, damaging the renal functions |
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When radiating a malignant tumor of retroperitoneum - what can happen to kidney?
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A side effect of radiation:
- Tumor is necrotic - Other tissue is atrophic: So kidney has a production of fibrous tissue - compressing the uretheres |
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3 types of kidney rejections?
(transplantation nephropathology) |
1. Humoral rejection
2. Acute cellular rejection 3. Chronic rejection ==> They are NOT dependent on each other! |
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Which is the most frequent type of kidney rejection?
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Cellular rejection
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Time span of humoral kidney rejection?
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Minutes - weeks after transplantatino
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How is kidney rejected in humoral rejection?
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Antibodies against graft - which activate complement system
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Histology of humoral rejection of kidney?
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1. Vasculitis
2. Thrombi in glomeruli |
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Time span of acute cellular rejection?
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1 week after
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What cells are rejecting the kidney in cellular rejection?
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T-cells
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Histology of cellular kidney rejection?
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- Lymphocytes in interstitium
- Lymphocytes in tubular epithelium (tubulitis) - Interstitial edema |
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What is the clinical manifestation of cellular rejection of kidney?
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1. Decreased renal functions
2. Azotemia (nitrogen metabolism) |
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Time span of chronic renal rejection?
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Months to years
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Gross appearance of chronic rejected kidney?
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Shrunken
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Histology of chronic rejected kidney?
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Thickened arterial intima leading to:
- Narrowed lumen and ischemia of graft |
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Clinical manifestations of chronic kidney rejection?
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1. Reduced GFR
2. Renal failure |
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What is the most common disease of the new graft?
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Membranous glomerulonephritis
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Which 2 diseases is guaranteed to get kidney disease again - even with new graft?
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1. Membranous glomerulonephritis
2. FSGS |
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What happens to kidney if it is a long time between 2 patients?
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Acute tubular necrosis
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What immunosuppresser do we use for patient with kidney transplantation?
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Cyclosporine A
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What is the side-effect of cyclosporine A?
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Toxic:
- Thickening of small arteries - Fibrosis of graft |
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Definition of acute tubular necrosis?
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Destruction of tubular cells, manifesting with acute renal failure and oliguria
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Definition oliguria?
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<500ml/day
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ATN can be classified into to etiologies?
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1. Ischemic
2. Toxic |
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Causes of ischemic ATN?
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Shock states:
- Hypoperfusion - Septicemia - Pancreatitis - Crush syndrome |
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How does Crush syndrome affect kidneys?
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1. Compression of skeletal muscles
2. Release of myoglobin which is precipitated in tubules |
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Etiologies of toxic ATN?
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- Heavy metals (mercury)
- Ethylenglycol (added to antifrost) - High dose ATB (gentamicin) - Pesticides |
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Pathogenesis of ATN?
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1. Tubular necrosis
2. Blockage of tubule due to necrotic debris (oliguria) 3. Fluid leak into interstitium - edema and tubular collapse |
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Gross appearance of kidney in ATN?
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Cortex - pale
Medulla - dark |
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Histology of ischemic type of ATN?
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- Necrosis of SHORT segments of proximal tubules
- Necrotic cells in tubules with Tamm-Horsfall protein => Together forming casts in collecting ducts |
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Why is only the proximal tubules affected in ischemic ATN?
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Most sensitive to oxygen shortage
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What is Tamm-Horsfall protein?
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A protein produced by tubular cells
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How does the casts look in LM?
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Granular
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So the casts in ATN consist of?
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1. Necrotized cells
2. Tamm-Horsfall protein |
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Histology of toxic type of ATN?
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The WHOLE of proximal tubule is necrotic - since here is the highest concentration of the toxins
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In ischemic type we also see tubulorrhexis. What is it?
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Rupture of tubular BM
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3 clinical stages of ATN and time span?
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1. Initiation - 1-2 days
2. Maintenance 2-6 days 3. Recovery - 1 week |
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What happens in initiation phase of ATN?
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Ischemia & azotemia
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What happens in maintenance phase of ATN?
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- Oliguria up to anuria (necrotic debris)
- High threat of uremia & water overload ==> Lethal without dialysis!! |
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What happens in recovery phase of ATN?
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Regeneration of renal tubular cells - as long as BM is undestroyed.
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Why is there polyuria in the recovery phase of ATN?
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Since the renewed tubular cells do not work properly in the start :-)
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Name a special type of ATN and what it is caused by?
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Massive cortical necrosis - caused by:
- Long term shock - DIC Leading to ATN like symptoms and hopeless prognosis. |
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In diabetic patient - which 4 lesions are expected?
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1. Glomerulosclerosis
2. Nephrosclerosis 3. Repeated pyelonephritis with necrotizing papillitis 4. Armani cells |
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How does DM cause glomerulosclerosis?
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Due to increased growth factors from the hyperglycemia - the glomerular BM thickens and mesangium increase
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Mesangium can increase in 2 ways - what are they?
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1. Diffuse
2. Nodular |
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Nodular increase in mesangium is called with a special name?
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Kimmelstiel-Wilson nodules
A hyalinized mesangial matrix |
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What does it mean that the mesangium is hyalinized?
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It just looks like that in LM - amorphous homogenous eosinophilic material
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What is nephrosclerosis of kidney - in DM?
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Accelerated atherosclerosis, affecting afferent and efferent arterioles
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What are the diseases involving vessels of the kidney?
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1. Renal artery stenosis
2. Kidney infarction 3. Arteriosclerotic nephrosclerosis 4. Hypertensive nephrosclerosis |
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Renal artery stenosis in old patients occur due to?
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Atherosclerosis
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Renal artery stenosis occur in young patients due to?
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Fibromuscular hyperplasia / dysplasia
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What is fibromuscular hyperplasia?
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Increased fibrous tissue and muscle cells in wall - leading to hypertension due to RAAS
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Long term renal artery stenosis will lead to?
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Kidney atrophy
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Which 4 sources may infarct the kidney?
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1. Infective endocarditis
2. Mural thrombosis post MI 3. Rupture of atheroma plaques of aorta 4. Thrombosis in polyarteritis nodosa |
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Definition atheroma?
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Lesion filled with porridge like material of:
- Macrophages - Lipids (together foamy cells) - Cholesterol etc.. |
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Where does arteriosclerosis affect in liver?
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Branches of renal arteries
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How does a kidney affected by arteriosclerosis look grossly?
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V-shaped scars (compared to U-shaped in chronic pyelonephritis)
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2 types of hypertensive nephrosclerosis?
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1. Benign nephrosclerosis
2. Malignant nephrosclerosis |
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Typical BP in benign nephrosclerosis?
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Maybe 150/95 - not very much
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What is malignant hypertension?
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200/110
Diastolic over 110 most important |
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Gross appearance of kidneys in hypertensive nephrosclerosis?
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Smaller
Granulated surface |
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Histology of kidney in benign nephrosclerosis?
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Hyaline thickening of arterioles - 'hyaline arteriosclerosis'
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Hyaline arteriosclerosis in benign nephrosclerosis lead to?
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Stenosis - ischemia and a mild atrophy.
No renal failure |
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Pathogenesis of malignant nephrosclerosis?
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Due to the high pressure fibrinogen enter the wall - leading to endothelial injury and fibrinous necrosis
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What is the reaction of the t. intima to the fibrinous necrosis in malignant nephrosclerosis?
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Hyperplasia of fibrocytes and fibrosis
Thickening, narrowing, more ischemia, higher BP… Circulus visciosus |
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How does larger arteries look in malignant hypertension?
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Onion-like proliferation of intimal cells
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How does arterioles look in malignant hypertension?
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Fibrinoid necrosis
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How does glomeruli of kidney look in malignant hypertension?
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- Segmental necrosis
- Crescents |
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What are the clinical manifestations of malignant hypertension?
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- Diastole higher than 110
- Papilledema - Encephalopathy - Renal failure |
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Which typical systemic vasculitises affect the kidney?
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1. Polyarteritis nodosa
2. Polyangitis microscopa 3. Granulomatosis with polyangitis (wegener) 4. Allergic granulomatosis (Churg-Strauss) 5. Thrombotic microangiopathies |
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Polyarteritis nodosa affect which kidney arteries?
Does it affect glomeruli? |
- Interlobular
- Arcuate Glomeruli are SPARED :) |
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Polyarteritis nodosa cause what in kidney?
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1. Fibrinoid necrosis
2. Inflammation 3. Thrombosis |
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Polyangitis microscopa affect which arteries in kidney?
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Small like:
- Afferent - Glomerular |
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Wegener's in kidney?
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Periglomarular granulomas
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Another name for wegener's granulomatosis?
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Granulomatosis with polyangitis
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Another name for allergic granulomatosis?
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Churg-Strauss syndrome
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How does Churg-Strauss syndrome affect kidneys?
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By focal segmental necrotizing glomerulonephritis
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Definition thrombotic microangiopathies?
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Thrombosis in the microcirculation
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Thrombotic microangiopathies manifest clinically as?
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- Hemolytic anemia
- Thrombocytopenia - Renal failure |
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2 diseases of thrombotic microangiopathies?
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HUS = Hemolytic uremic syndrome
TTP = Thrombotic thrombocytopenic purpura |
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What is HUS?
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E-coli cause endothelial damage, leading to thrombosis in renal microcirculation and renal failure
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What is the main cause of renal failure in children?
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HUS
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What is TTP / thrombotic thrombocytopenic purpura?
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Acquired defect in cleavage of von Willebrant factor - so thrombosis occur.
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What are the 3 main types of urinary stones?
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1. Calcium oxalate (phosphate) (80%)
2. Triple phosphate 3. Uric acid / cysteine |
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What are the most important causes of urinary stone formation?
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1. Increased concentration of stone consituents
2. Alkaline urine due to UTI (triple phosphate depos.) |
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Clinically 2 outcomes of urinary stones?
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1. Very big stones is stuck in pelvis causing pyelonephritis (staghorn)
2. Small stones enter ureters (hydronephrosis) Also hematuria & colic pain |
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What is hydronephrosis?
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Renal parenchyma atrophy, due to dilation of renal pelvis due to urine outflow obstruction
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What clinical syndromes are associated with renal failure?
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Azotemia / uremia
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Prerenal causes of renal failure?
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1. Shock hypoperfusion
2. Centralization of perfusion 3. Obstructions? |
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Renal causes of renal failure?
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Parenchymal diseases
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Postrenal causes of renal failure?
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Obstruction of both ureters
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Manifestation of uremia in sudden renal failure?
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Hyperkalemia, arrhytmia and death
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Manifestations of uremia in acute to long term renal failure?
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- Hairy heart
- Hairy pleura - Uremic lung - Uremic encephalopathy - Crying stomach - Treit's pseudomembranous colitis |
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What is hairy heart?
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Fibrinous pericarditis:
- Fibrin deposited on surface of heart due to increased permeability to fibrin |
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Another name for fibrinous pericarditis?
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Cor villosum (hairy heart)
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What is uremic lung?
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Lung edema with hyaline membranes lining alveoli (acute ARDS?)
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What is uremic encephalopathy?
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Brain edema due to uremia - with seizures and sleepiness
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What is a 'crying stomach'?
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A hemorrhagic gastritis with inflammation, edema and bleeding of gastric mucosa
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What is Treit's pseudomembranous colitis?
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A thin layer of fibrin on mucosa of colon
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What are the uremic manifestations of long term renal failure?
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- Anemia
- Grey skin - Renal osteopathy - Hypercalcemia - Increased bleeding - Metabolic acidosis |
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Why anemia in long term renal failure?
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Lower EPO production
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Why renal osteopathy in long term renal failure?
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Low vit D metabolism
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Why does the skin become grey in long term renal failure?
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Due to deposition of urine pigment and anemia
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Why is there hypercalcemia in long term renal failure?
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Due to secondary hyperparathyroidism - due to lower vit D
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Why is there metabolic acidosis in long term renal failure?
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1. Lower H+ secretion
2. Lower HCO3- absorption |
